The present invention relates in general to a method for achieving haemostasis by applying an external compression pressure on a puncture wound in combination with a coagulant treatment of said puncture wound. The invention also relates to a device with which the coagulant and the external compression pressure can be applied simultaneously on the puncture wound.
Following an invasive medical procedure, such as catheterisation or similar invasive medical procedure, the flow of blood through the puncture wound has to be stopped, so that haemostasis can begin as soon and fast as possible after the completion of the invasive medical procedure. Several devices have been suggested that facilitate and accelerate this haemostasis by providing a compression pressure that compresses the blood vessels at the puncture site to stop the flow of blood therethrough. Examples of femoral compression devices may be found in the U.S. Pat. Nos. 4,957,105, 5,307,811, 5,799,650 and 5,997,564, while examples of devices for the compression of the radial artery may be found in U.S. Pat. Nos. 4,798,199, 5,569,297 and 5,601,597. The entire contents of all of these patents are incorporated herein by reference.
Although there exist numerous compression devices having very different designs and types of mechanical or pneumatical pressure applying means, the basic working principle is the same: a pressure element is positioned at the wound site and some kind of compressing means is provided which presses the pressure element against the puncture wound, thereby stopping the flow of blood therethrough so that haemostasis can begin. Normally it takes about 20 minutes to achieve haemostasis. If, however, a patient has been given heparin to, for example, avoid blood clots, the time for achieving haemostasis may be as long as 1.5 hours. Besides being uncomfortable for the patient and being expensive for the medical service, a long compression time involves the risks of vein thrombosis, tissue necrosis, nervous damages, and other more or less severe complications.
In the case described above, the underlying process for haemostasis is the so-called normal clotting mechanism, which basically involves three steps: 1) a complex substance called prothrombin activator is formed, 2) prothrombin activator converts a plasma protein called prothrombin into thrombin, and 3) thrombin catalyses the joining of fibrinogen molecules present in plasma to a fibrin mesh, which traps blood cells and effectively seals the wound until the blood vessel can be permanently repaired (see E. N. Marieb, Human Anatomy and Physiology, 3rd ed., The Benjamin/Cummings Publishing Company, CA, 1995, p. 601).
Since it takes a certain amount of time before haemostasis is achieved by means of the normal clotting mechanism, there also exists a corresponding minimal compression time, i.e. the time during which the compression device has to be arranged around a part of the patient""s body. This compression time is, of course, dependent on several different factors, which vary from patient to patient, such as the specific puncture site and size, different blood related parameters, if heparin or some other anticoagulants are used, etc. Nevertheless, for a given patient, a minimal compression time exists for achieving haemostasis.
In order to further reduce the compression time, a compression device can be combined with some other means that produces haemostasis via a mechanism which is different from the normal clotting mechanism. Such a haemostatic agent is chitosan, which is a collective term applied to deacetylated chitins in various stages of deacetylation and depolymerisation. Chitin is the structural polymer of the exoskeleton of arthropods and cell walls of fungi. These are linked by Beta 1-4 glycosidic bonds into a linear polymer containing hundreds or thousands of units. The technology for the preparation of chitosan is described in U.S. Pat. No. 3,533,940. The entire contents of this patent are incorporated herein by reference. Several studies have shown that chitosan achieves haemostasis independent of normal clotting mechanisms via cellular aggregation or clogging (see P. R. Klokkevold, The Effect of Poly-N-Acetyl Glucosaminoglycan (Chitosan) on Osteogenesis in vitro, Thesis, UCLA, LA, 1995). Herein the mechanism(s) with which chitosan is achieving haemostasis is referred to as the clogging mechanism.
By providing the pressure element of a compression device with an active layer of chitosan, it is therefore possible to combine the normal clotting mechanism and the clogging mechanism, thereby reducing the time during which the compression device has to be arranged around a part of the patient""s body. This combined method can be extremely valuable when the normal clotting mechanism is absent or reduced due to, for example, a heparin treatment of the patient.
The present invention thus provides a method for achieving haemostasis, wherein the normal clotting mechanism is combined with the chitosan induced clogging mechanism. The invention also provides a method for achieving haemostasis when the effect of the normal clotting mechanism is reduced or absent. Chitosan and an external compression pressure can be applied simultaneously on a puncture wound.
A compression device according to the present invention comprises a compressor connected to a pressure element having a side provided with chitosan. The compressor may comprise an adjustable belt or clamp to be arranged around a part of the patient""s body. In use, the chitosan side of the pressure element is placed in contact with the puncture wound, and the compressor is operated for applying an external compression pressure on the pressure element, which, in turn, presses against the puncture wound. The chitosan is released into the blood and tissue of the patient, and it is therefore possible to obtain haemostasis by means of the combined effects of the normal clotting mechanism and the clogging mechanism, thereby reducing the time during which the compression device has to be arranged around a part of the patient""s body.